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Zhu D, Zhang X, Wang F, et al. Irisin rescues diabetic cardiac microvascular injury via ERK1/2/Nrf2/HO-1 mediated inhibition of oxidative stress. Diabetes Res Clin Pract. 2021;183:109170doi: 10.1016/j.diabres.2021.109170.
Zhu, D., Zhang, X., Wang, F., Ye, Q., Yang, C., & Liu, D. (2021). Irisin rescues diabetic cardiac microvascular injury via ERK1/2/Nrf2/HO-1 mediated inhibition of oxidative stress. Diabetes research and clinical practice, 183109170. https://doi.org/10.1016/j.diabres.2021.109170
Zhu, Di, et al. "Irisin rescues diabetic cardiac microvascular injury via ERK1/2/Nrf2/HO-1 mediated inhibition of oxidative stress." Diabetes research and clinical practice vol. 183 (2021): 109170. doi: https://doi.org/10.1016/j.diabres.2021.109170
Zhu D, Zhang X, Wang F, Ye Q, Yang C, Liu D. Irisin rescues diabetic cardiac microvascular injury via ERK1/2/Nrf2/HO-1 mediated inhibition of oxidative stress. Diabetes Res Clin Pract. 2021 Dec 02;183:109170. doi: 10.1016/j.diabres.2021.109170. Epub 2021 Dec 02. PMID: 34863716.
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Diabetes Res Clin Pract. 2021 Dec 02;183:109170. doi: 10.1016/j.diabres.2021.109170. Epub 2021 Dec 02.

Irisin rescues diabetic cardiac microvascular injury via ERK1/2/Nrf2/HO-1 mediated inhibition of oxidative stress.

Diabetes research and clinical practice

Di Zhu, Xiaotian Zhang, Fenglin Wang, Qiao Ye, Caizhe Yang, Demin Liu

Affiliations

  1. Department of Endocrinology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing 100142, China.
  2. Hospital of Troop 75600, 3002 Fuqiang Road, Shenzhen 518048, China.
  3. Clinical Medicine Laboratory, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing 100142, China.
  4. Department of Endocrinology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing 100142, China. Electronic address: [email protected].
  5. Department of Cardiology, Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang 050010, China. Electronic address: [email protected].

PMID: 34863716 DOI: 10.1016/j.diabres.2021.109170

Abstract

AIMS: Cardiac microvascular dysfunction is a common feature across cardiovascular complications in diabetes, while effective therapy remains elusive. This study was designed to evaluate the effect of irisin on cardiac microvascular injury in type 2 diabetes mellitus (T2DM).

METHODS: T2DM was induced in C57BL/6J mice. A cohort diabetic mice received a 12-week treatment of irisin. Cardiac function and microvessel density were evaluated. Whether irisin directly regulates cardiac microvascular endothelial cells (CMECs) function was determined in vitro. Discovery-drive approaches followed by cause-effect analysis were used to uncover the molecular mechanisms.

RESULTS: Irisin improved cardiac function in diabetic mice, and increased microvessel density. In vitro study revealed that irisin promoted CMECs proliferation and reduced high glucose and high lipid (HGHL)-induced apoptosis. Mechanistically, irisin increased mRNA and protein levels of heme oxygenase 1 (HO-1), superoxide dismutase 1 and superoxide dismutase 2, among which HO-1 ranked top. Irisin stimulated the phosphorylation of extracellular regulated protein kinases (ERK) 1/2 and nuclear factor erythroid-derived 2-like 2 (Nrf2) nuclear translocation, while U0126 (the inhibitor of ERK1/2) inhibited irisin-induced Nrf2 nuclear translocation and HO-1 expression. Nrf2 siRNA inhibited irisin's antioxidative effects.

CONCLUSION: Irisin could rescue cardiac microvessels against oxidative stress and apoptosis in diabetes via ERK1/2/Nrf2/HO-1 pathway.

Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.

Keywords: Cardiac microvascular injury; Irisin; Oxidative stress; Type 2 diabetes mellitus

Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this pa

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